Skip to main content

Overexpression of cyclooxygenase-2 in urothelial carcinoma in conjunction with tumor-associated-macrophage infiltration, hypoxia-inducible factor-1α expression, and tumor angiogenesis

Buy Article:

$51.00 plus tax (Refund Policy)

Abstract:

Chen W-T, Hung W-C, Kang W-Y, Huang Y-C, Su Y-C, Yang C-H, Chai C-Y. Overexpression of Cyclooxygenase-2 in Urothelial Carcinoma: in conjunction with tumor-associated-macrophage infiltration, hypoxia-inducible factor-1α expression, and tumor angiogenesis. APMIS 2009; 117:176–84.

This study examines whether the expression of cyclooxgenase-2 (COX-2) in urothelial carcinoma (UC) is associated with macrophage infiltration, hypoxia-inducible factor-1α (HIF-1α) expression and angiogenesis. We investigated the expression of COX-2 associated with HIF-1α and performed double immunohistochemical analysis of 216 UCs for COX-2 expression and the correlation with tumor-associated-macrophage (TAM) density and microvessel density (MVD) in situ. A high expression of COX-2 was positively correlated with tumor invasiveness, histologic grade and HIF-1α expression in UC (p<0.0001, p=0.003, p<0.0001, respectively). Quantification of double staining of COX-2/CD34 and COX-2/CD68 showed that a higher MVD and TAM density was found in COX-2 high-expression than in COX-2 low-expression tumor fields (p<0.0001). Adjacent to the principal of COX-2 expression areas, MVD value and TAM density were significantly increased in HIF-1α high-expression specimens compared with HIF-1α low-expression ones (p<0.0001). Interestingly, our data revealed that high COX-2 expression (p=0.002), high HIF-1α expression (p<0.0001) and TAM density (p<0.0001) were all associated with high MVD value. Our results suggest that COX-2 may produce a cooperative effect in promoting tumor progression and may be involved in the process of angiogenesis through increasing TAM infiltration or HIF-1α regulation by hypoxia.

Keywords: Urothelial carcinoma; hypoxia-inducible factor-1α; immunohistochemistry; microvessel density; tumor-associated-macrophage

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1600-0463.2008.00004.x

Affiliations: Department of Pathology, Kaohsiung Medical University Hospital, Kaohsiung;

Publication date: March 1, 2009

Access Key

Free Content
Free content
New Content
New content
Open Access Content
Open access content
Subscribed Content
Subscribed content
Free Trial Content
Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more